1214 Part VII / Development and the Emergence of Behavior
Figure 49–2 Afferent pathways from the two eyes project
to discrete columns of neurons in the visual cortex.Retinal
ganglion neurons from each eye send axons to separate
layers of the lateral geniculate nucleus. The axons of neurons
in this nucleus project to neurons in layer IVC of the primary
visual cortex, which is organized in alternating sets of ocular
dominance columns; each column receives input from only one
eye. The axons of the neurons in layer IVC project to neurons in
adjacent columns as well as to neurons in the upper and lower
layers of the same column. As a result, most neurons in the
upper and lower layers of the cortex receive information from
both eyes.
pathway to determine where the defect arose (Figure
49–2). They found that retinal ganglion cells in the
deprived eye, as well as neurons in the lateral genicu-
late nucleus that receive input from the deprived eye,
responded well to visual stimuli and had essentially
normal receptive fields.
In contrast, cells in the visual cortex were fun-
damentally altered. In the cortex of normal animals,
most neurons are responsive to binocular input. In
animals that had been monocularly deprived for the
first 6 months, most cortical neurons did not respond
to signals from the deprived eye (Figure 49–3). The few
cortical cells that were responsive were not sufficient
for visual perception. Not only had the deprived eye
lost its ability to drive most cortical neurons, but little
recovery ever occurred: The loss was permanent and
irreversible.
Hubel and Wiesel went on to test the effects of
visual deprivation imposed for shorter periods and
at different ages. They obtained three types of results,
depending on the timing and duration of the depri-
vation. First, monocular deprivation for a few weeks
shortly after birth led to loss of cortical responses from
the deprived eye that was reversible after the eye had
been opened, especially if the opposite eye was then
closed to encourage use of the initially deprived eye.
Second, monocular deprivation for a few weeks dur-
ing the next several weeks also resulted in a substan-
tial loss of cortical responsiveness to signals from the
deprived eye, but in this case, the effects were irrevers-
ible. Finally, deprivation in adults, even for periods of
左眼
右眼
左大脑半球
视觉皮层
外侧膝状体
视束
视神经
视交叉
左眼
右眼
岛前庭
皮层
many months, had no effect on the responses of cortical
cells to signals from the deprived eye or on visual per-
ception. These results demonstrated that the cortical
connections that control visual perception are estab-
lished within a critical period of early development.
Are there anatomical correlates of these functional
defects? To address this question, we need to recall
three basic facts about the anatomy of the visual cortex
(Figure 49–2). First, inputs from the two eyes remain
segregated in the lateral geniculate nucleus. Second,
the geniculate inputs carrying information from the
two eyes to the cortex terminate in alternating col-
umns, termed ocular dominance columns. Third, lateral
geniculate axons terminate on neurons in layer IVC of
the primary visual cortex; convergence of input from
the two eyes on a common target cell occurs at the
next stage of the pathway, in cells above and below
layer IVC.
To examine whether the architecture of ocular dom-
inance columns depends on visual experience early in
postnatal life, Hubel and Wiesel deprived newborn
animals of vision in one eye and then injected a labeled
amino acid into the normal eye. The injected label was
incorporated into proteins in retinal ganglion cell bod-
ies, transported along the retinal axons to the lateral
geniculate nucleus, transferred to geniculate neurons,
and then transported to the synaptic terminals of these
axons in the primary visual cortex. After closure of one
eye, the columnar array of synaptic terminals relaying
input from the deprived eye was reduced, whereas the
columnar array of terminals relaying input from the
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